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Developmental changes in the sensitivity of the chick embryo ventricle to beta-adrenergic agonist during adrenergic
Insights
Chick embryo ventricles show decreased sensitivity to isoproterenol (Iso) during development. This subsensitivity is not caused by adrenergic nerve activity, suggesting other regulatory mechanisms are involved in beta-adrenergic agonist response.
Area of Science:
- Developmental biology
- Pharmacology
- Cardiovascular physiology
Background:
- Chick embryo ventricles exhibit a positive inotropic response to isoproterenol (Iso) from the 4th embryonic day.
- Adrenergic neurotransmission plays a role in regulating cardiac contractility during embryonic development.
Purpose of the Study:
- To investigate the developmental changes in chick embryo ventricular sensitivity to isoproterenol (Iso).
- To determine if adrenergic nerve activity contributes to the transient subsensitivity to Iso observed during embryonic development.
Main Methods:
- Measurement of isometric contractile force and tension development in isolated chick embryo right ventricles.
- Administration of isoproterenol (Iso) at various embryonic ages.
- Pharmacological manipulation using reserpine and 6-hydroxydopamine to assess adrenergic nerve involvement.
Main Results:
- A transient, 10-fold decrease in Iso sensitivity (increased ED50) was observed between the 16th and 21st embryonic days.
- Adrenergic nerves became capable of altering ventricular contractility on the 16th embryonic day.
- Reserpine and 6-hydroxydopamine treatments did not affect Iso subsensitivity or normal heart weight development.
Conclusions:
- The local release of transmitter from adrenergic nerves does not cause the transient subsensitivity of the chick embryo ventricle to beta-adrenergic agonists.
- Other mechanisms likely regulate the developmental changes in beta-adrenergic receptor responsiveness in the embryonic chick heart.
Abstract:
As early as the 4th embryonic day, the ventricle of the chick embryo responded to isoproterenol (Iso) with an increase in the force of contraction; at all ages studied, this positive inotropic effect was accompanied by an increased rate of tension development. There was a transient, 10-fold decrease in the sensitivity (increase in ED50) of the right ventricle to Iso between the 16th and 21st embryonic day. This change in the sensitivity to Iso was not due either to an increased inactivation of Iso by non-neuronal cells or to a change in the thickness of the ventricle. It was found that adrenergic nerves were first capable of altering ventricular contractility on the 16th embryonic day. Whereas they interfered with the function of adrenergic nerves, injections of reserpine or 6-hydroxydopamine had no effect on the subsensitivity to Iso. Furthermore, these agents did not affect the normal developmental changes in heart weight. We conclude that the local release of transmitter from adrenergic nerves does not cause the transient subsensitivity of the ventricle of the chick embryo to beta-adrenergic agonists.